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  • Ca2+-activated K+ channels  (1)
  • DIDS  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Intracellular pH during secretion in the perfused rabbit mandibular salivary gland measured by31P NMR spectroscopy (1989)
    Springer
    Pflügers Archiv 414 (1989), S. 200-207 
    Details
    ISSN: 1432-2013
    Keywords: Salivary gland ; Intracellular pH ; 31P NMR spectroscopy ; Acetylcholine ; Amiloride ; DIDS ; Na+−H+ exchange
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Intracellular pH (pHi) was measured in the isolated, perfused rabbit mandibular salivary gland by31P NMR spectroscopy. In the unstimulated gland perfused with HCO 3 − /CO2-buffered Ringer's solution, pHi was 7.27±0.01. Continuous stimulation with acetylcholine elicited dose- and time-dependent changes in pHi. 10−6 mol/l acetylcholine caused a brief intracellular acidosis (−0.19±0.06 pH units) followed by an increase in pHi to a more alkaline steady-state value (7.33±0.02). In the absence of perfusate HCO 3 − or in the presence of 10−4 mol/l DIDS (4,4′-diisothiocyanatostilbene-2,2′-disulphonic acid), the transient acidosis was abolished and pHi increased rapidly to give a sustained alkalosis (7.49±0.03 and 7.44±0.03 respectively). In the presence of 10−3 mol/l amiloride, the response to acetylcholine was a rapid decrease in pHi to 7.02±0.02. The data suggest that, during perfusion with HCO 3 − /CO2-buffered solutions, stimulation with acetylcholine results in a transient loss of HCO 3 − from the acinar cells (causing a transient acidosis), and, independently, the activation of Na+−H+ exchange (causing a sustained alkalosis). In the unstimulated gland, DIDS and the HCO 3 − -free perfusate caused decreases in pHi to 7.12±0.02 and 7.04±0.01 respectively. In contrast, amiloride had little effect. The relatively high value of pHi maintained by the unstimulated gland is therefore probably not due to Na+−H+ exchange.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00580964
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  • 2
    Electronic Resource
    Electronic Resource
    Basolateral K+ efflux is largely independent of maxi-K+ channels in rat submandibular glands during secretion (1994)
    Springer
    Pflügers Archiv 428 (1994), S. 516-525 
    Details
    ISSN: 1432-2013
    Keywords: Ca2+-activated K+ channels ; Maxi-K+ channel ; Tetraethylammonium ; Salivary gland ; Fluid secretion ; K+ efflux ; Epithelial transport
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The involvement of large-conductance, voltage- and Ca2+-activated K+ channels (maxi-K+ channels) in basolateral Ca2+-dependent K+-efflux pathways and fluid secretion by the rat submandibular gland was investigated. Basolateral K+ efflux was monitored by measuring the change in K+ concentration in the perfusate collected from the vein of the isolated, perfused rat submandibular gland every 30 s. Under conditions in which the Na+/K+-ATPase and Na+-K+-2Cl− cotransporter were inhibited by ouabain (1 mmol/l) and bumeta-nide (50 μmol/l) respectively, continuous stimulation with acetylcholine (ACh) (1 μmol/l) caused a transient large net K+ efflux, followed by a smaller K+ efflux, which gradually returned to the basal level within 10 min. These two components of the K+ efflux appear to be dependent on an increase in cytosolic Ca2+ concentration. The initial transient K+ efflux was not affected by charybdotoxin (100 nmol/l) or tetraethylammonium (TEA) (5 mmol/l) but the smaller second component was strongly and reversibly inhibited by charybdotoxin (100 nmol/l) and TEA (0.1 and 5 mmol/l). The initial K+ efflux transient induced by ACh was inhibited by quinine (0.1–3 mmol/l), quinidine (1–3 mmol/l) and Ba2+ (5 mmol/l), but not by verapamil (0.1 mmol/l), lidocaine (1 mmol/l), 4-aminopyridine (1 mmol/l) or apamin (1 μmol/l). Ca2+-dependent transient large K+ effluxes induced by substance P (0.01 μmol/l) and A23187 (3 μmol/l) were not inhibited by TEA (5 mmol/l or 10 mmol/l). A23187 (3 μmol/l) evoked a biphasic fluid-secretory response, which was not inhibited by TEA (5 mmol/l). Patch-clamp studies confirmed that the whole-cell outward K+ current attributable to maxi-K+ channels obtained from rat submandibular endpiece cells was strongly inhibited by the addition of TEA (1–10 mmol/l) to the bath. It is concluded that maxi-K+ channels are not responsible for the major part of the Ca2+-dependent basolateral K+ efflux and fluid secretion by the rat submandibular gland.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00374573
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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